title: Asymmetric dimethylarginine serum levels in non-diabetic ankylosing spondylitis patients undergoing TNF-α antagonist therapy.
abstract: OBJECTIVE
  This paper aims to determine whether disease activity, systemic inflammation and metabolic syndrome are potential determinants of circulating asymmetric dimethylarginine (ADMA) in ankylosing spondylitis (AS) patients undergoing TNF-α antagonist-infliximab-therapy.
  
  
  METHODS
  We investigated ADMA serum concentrations in a series of 30 non-diabetic AS patients without history of cardiovascular (CV) events that were treated with the TNF-α antagonist infliximab, immediately prior to an infliximab infusion. Correlations of ADMA serum levels with disease activity, systemic inflammation and metabolic syndrome were assessed. Also, potential changes in ADMA concentration following an infusion of the anti-TNF-α monoclonal antibody-infliximab were analysed.
  
  
  RESULTS
  A higher concentrations of ADMA in men (p=0.012) and patients with hypertension was found (p=0.001). There was also a marginally positive correlation of ADMA serum levels with C-reactive protein levels (p=0.08). Moreover, a significant negative correlation between ADMA levels and total cholesterol and LDL-cholesterol was observed (p= 0.05). No differences in ADMA levels according to the specific clinical features of the disease were seen. A single infliximab infusion did not lead to significant changes in ADMA serum levels.
  
  
  CONCLUSIONS
  In AS patients undergoing periodical treatment with the anti-TNF-α monoclonal antibody-infliximab a link between some features of metabolic syndrome and ADMA concentrations was observed.
authors.affiliation: Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Rheumatology Division, IFIMAV, Santander, Spain. fernandagenre@gmail.com.
authors.forename: Fernanda
authors.initials: F
authors.lastname: Genre
authors.forename: Raquel
authors.initials: R
authors.lastname: López-Mejías
authors.forename: Jose A
authors.initials: JA
authors.lastname: Miranda-Filloy
authors.forename: Beatriz
authors.initials: B
authors.lastname: Carnero-López
authors.forename: Inés
authors.initials: I
authors.lastname: Gómez-Acebo
authors.forename: Ricardo
authors.initials: R
authors.lastname: Blanco
authors.forename: Rodrigo
authors.initials: R
authors.lastname: Ochoa
authors.forename: Javier
authors.initials: J
authors.lastname: Rueda
authors.forename: Carlos
authors.initials: C
authors.lastname: González-Juanatey
authors.forename: Javier
authors.initials: J
authors.lastname: Llorca
authors.forename: Miguel A
authors.initials: MA
authors.lastname: González-Gay
mesh_terms: D000328:Adult; D000368:Aged; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D000911:Antibodies, Monoclonal / Q000008:administration & dosage / Q000627:therapeutic use*; D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood; D015415:Biomarkers / Q000097:blood; D005260:Female; D006801:Humans; D000069285:Infliximab; D007262:Infusions, Intravenous; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood* / Q000276:immunology; D008875:Middle Aged; D013167:Spondylitis, Ankylosing / Q000097:blood / Q000188:drug therapy* / Q000276:immunology; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D015415:Biomarkers; D014409:Tumor Necrosis Factor-alpha; C018524:N,N-dimethylarginine; D001120:Arginine; D000069285:Infliximab